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Differentiation of a Human Neural Stem Cell Line on Three Dimensional Cultures, Analysis of MicroRNA and Putative Target Genes
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Silencing CASC11 curbs neonatal neuroblastoma progression through modulating microRNA-676-3p/nucleolar protein 4 like

Zekun Yu1, Jing Zhang1, Jun Han2

  • 1Department of Neonatology, the First Hospital of Jilin University, No. 71, XinMin Street, Changchun, 130021, Jilin, China.

Pediatric Research
|October 24, 2019
PubMed
Abstract

Insights

Long non-coding RNA CASC11 promotes neonatal neuroblastoma by sequestering miR-676-3p, inhibiting NOL4L. Targeting CASC11 offers a potential therapeutic strategy for this cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Neuroblastoma is the most common extracranial solid cancer in neonates.
  • Long non-coding RNA cancer susceptibility 11 (CASC11) is implicated in various cancers, but its role in neonatal neuroblastoma is unclear.

Purpose of the Study:

  • To investigate the role of CASC11 in neonatal neuroblastoma.
  • To elucidate the molecular mechanism of CASC11 in regulating neonatal neuroblastoma progression.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) for gene expression analysis.
  • Cell proliferation, migration, and invasion assays (colony-formation, CCK-8, Transwell, wound-healing).
  • Molecular interaction studies including RNA pull-down, luciferase reporter, and RIP assays.

Main Results:

  • CASC11 expression is significantly upregulated in neonatal neuroblastoma tissues and cells.
  • High CASC11 levels correlate with poor patient survival.
  • CASC11 depletion inhibits proliferation and invasiveness; CASC11 acts as a molecular sponge, releasing NOL4L from miR-676-3p inhibition.

Conclusions:

  • CASC11 promotes neonatal neuroblastoma progression by sequestering miR-676-3p and upregulating NOL4L.
  • CASC11 represents a potential therapeutic target for neonatal neuroblastoma.

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